ID: 169. Issue 1 (November 2015)

• Record Type: Journal Article
• Authors: Weber, Friedemann
• Is Part Of: Cytokine. Volume 76:Issue 1(2015)
• Page Start: 63
• Publication Date: 2015-11
• Subjects: Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2015.08.034
• Languages: English
• ISSNs: 1043-4666

Abstract

<abstract xml:lang="en" abstract-type="author" id="ab005"> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <p id="sp005">Release of nucleocapsids into the cytoplasm is one of the first steps of virus infection. At this initial stage, viral copy numbers are low and the nucleocapsids are especially vulnerable to host cell defences.</p> <p id="sp010">The group of negative-stranded RNA viruses with a segmented genome (s-NSVs) contains several important pathogens like influenza virus (family Orthomyxoviridae), Rift Valley fever virus (genus phlebovirus, family Bunyaviridae), or Lassa virus (family Arenviridae). We have previously shown that the "panhandle" promoter of incoming s-NSV nucleocapsids is recognized by RIG-I, the main cytoplasmic pathogen sensor for RNA viruses. On one hand, this triggers antiviral signalling and IFN induction as expected. On the other hand, however, the clamping of RIG-I onto the "panhandle" promoter can exert a direct inhibitory effect on virus propagation. In my presentation, I will sum up these findings, present virus countermeasures, and expand the concept of immediate early nucleocapsid recognition beyond RIG-I.</p> </sec> </abstract>